Triiodothyronine attenuates estradiol-induced increases in dopamine D-2 receptor number in rat anterior pituitary
Jazyk angličtina Země Nizozemsko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
8705298
DOI
10.1016/0006-8993(95)01524-8
PII: 0006-8993(95)01524-8
Knihovny.cz E-zdroje
- MeSH
- adenohypofýza účinky léků metabolismus MeSH
- AMP cyklický metabolismus MeSH
- antagonisté estrogenu farmakologie MeSH
- krysa rodu Rattus MeSH
- potkani Wistar MeSH
- prolaktin metabolismus MeSH
- receptory dopaminu D2 účinky léků metabolismus MeSH
- thyreotropin metabolismus MeSH
- thyroxin metabolismus MeSH
- trijodthyronin farmakologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- AMP cyklický MeSH
- antagonisté estrogenu MeSH
- prolaktin MeSH
- receptory dopaminu D2 MeSH
- thyreotropin MeSH
- thyroxin MeSH
- trijodthyronin MeSH
Estrogens promote adenohypophyseal enlargement and tumor transformation, and thyroid hormones antagonize these effects. Hormone-induced pituitary enlargement may be mediated by alterations in pituitary dopaminergic function. The present study examined the effects of chronic (20 days) administration of estradiol benzoate (EB), triiodothyronine (T3), or EB and T3 (T3 + EB) on dopamine (D-2) receptors in rat anterior pituitary. D-2 receptor number increased after EB without altered receptor affinity. T3 alone did not affect D-2 receptor number in the anterior pituitary but significantly attenuated the effect of EB. T3 administration also inhibited EB-induced anterior pituitary hyperplasia. D-2 receptor upregulation by EB more likely could reflect a compensatory response to decreased receptor occupation. The present results suggest that D-2 receptors could play an important role in estrogen-induced adenohypophyseal tumor formation and hyperprolactinemia and that thyroid hormones may inhibit estrogen-induced pituitary tumor development via adenohypophyseal D-2 receptors.
Citace poskytuje Crossref.org
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